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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two cases of fetal tachyarrhythmias were treated in utero. One case showed supraventricular tachycardia which was successfully treated with procainamide. The other case was an atrial flutter with 2:1 atrioventricular conduction (AVC) which was treated with digoxin and verapamil. In both cases, the blood flow in the descending aorta was observed using pulsed Doppler ultrasound during therapy. In the first case, the interval of blood flow peaks was suddenly prolonged to normal heart rate, and in the second case, the blood flow peaks appeared irregularly which indicated that (AVC) was intermittently blocked. The blood flow pattern represented the mode of cardioversion. The blood flow velocity was also measured in both cases; it decreased transiently during therapy representing a depression in cardiac function. The cause of this was thought to be the negative inotropic effects of procainamide and verapamil. In spite of these negative inotropic effects, a greater R-R interval means a greater stroke volume. This relationship has a favorable effect on the fetal circulation as a result of therapy for fetal tachyarrhythmias.
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PMID:Hemodynamic changes during cardioversion in utero: a case report of supraventricular tachycardia and atrial flutter. 845 47

A 77-year-old male had been noticing progressive weakness of the legs for three years. By the age of 75 he had difficulty in climbing stairs. On admission, serum level of CPK was moderately high. There were weakness and atrophy of the proximal muscles. Deep tendon reflexes were depressed. Sensation was normal. The electromyogram and the biopsy of the femoral quadriceps muscles showed nonspecific changes. In 1989, he developed difficulty in walking and had congestive heart failure. On the second admission, moist rales were heard over the chest, and pitting edema was present in the lower extremities. The chest roentgenogram showed a cardiothoracic ratio of 63% and bilateral pleural effusion. The electrocardiogram showed atrial flutter with 2:1 conduction, QS in V1-3, rS in V4, and ST depression and T inversion in V5,6. The echocardiogram revealed a thick left ventricular wall and impaired left ventricular contraction (EF 22%). Macroglossia, hepatosplenomegaly and renal dysfunction were not noted. Congestive heart failure progressed and he suddenly died of ventricular tachycardia in December 1989. At autopsy, skeletal muscle fibers varied in size and showed fiber splitting. A cellular infiltration was observed in the stroma. Amyloid deposit was positively stained with Congo red. The heart weight was 570 g with marked left ventricular hypertrophy and moderate bilateral atrial dilatation. In both atria and ventricles, extensive amyloid deposition was found around myocardial fibers as well as in perivascular spaces. Amyloid was present also in the liver, the kidneys, the gastrointestinal tracts, and the other organs.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of primary systemic amyloidosis with skeletal muscle atrophy and congestive heart failure]. 848 88

Adenosine is a purine nucleoside with a rapid onset and brief duration of action after intravenous bolus administration. Its most prominent cardiac effect is impairment or blockade of atrioventricular nodal conduction, but other effects are depression of automaticity of the sinus node and attenuation of catecholamine-related ventricular after-depolarizations. The cardiac cell surface receptor is the A1 purinoceptor. The therapeutic value of adenosine is predominantly in those arrhythmias in which the atrioventricular node forms part of a reentry circuit, as clearly demonstrated by the high success rate for termination of atrioventricular nodal reentry tachycardia and of atrioventricular reentry tachycardia involving an accessory pathway in the Wolff-Parkinson-White syndrome. Ventricular tachycardias are generally unresponsive, with the exception of right ventricular outflow tract tachycardia. A diagnostic role has emerged for adenosine. The transient blockade of the atrioventricular node that it causes can reveal important electrocardiographic features in arrhythmias, such as atrial flutter, or can unmask latent preexcitation. In wide-QRS tachycardias, adenosine can help to distinguish ventricular tachycardia from supraventricular tachycardia with QRS aberration. Unlike verapamil, adenosine is safe in ventricular tachycardia. A suggested dosing scheme is to give incremental doses at 1-minute intervals, starting at 0.05 mg/kg and continuing until complete atrioventricular block is induced or a maximum of 0.25 mg/kg is reached. Side effects are transient, sometimes uncomfortable, and not hazardous; dyspnea and chest discomfort are most frequent. A history of asthma is a relative contraindication. Aminophylline antagonizes and dipyridamole potentiates the effects of adenosine.
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PMID:The therapeutic and diagnostic cardiac electrophysiological uses of adenosine. 848 69

1. By use of patch-clamp techniques, the effects of SD-3212, a novel antiarrhythmic drug, on the calcium current (Ica), the sodium current (INa) and the muscarinic acetylcholine-receptor-operated potassium current (IK.ACh) were examined and compared with those of bepridil in guinea-pig single atrial cells. 2. SD-3212 inhibited ICa and INa in a concentration-dependent manner. The IC50 values of SD-3212 for inhibition of ICa and INa were 1.29 microM and 3.92 microM, respectively. The steady state inactivation curves of ICa and INa were shifted in the hyperpolarizing direction in the presence of 1 microM SD-3212. Similar inhibition of ICa and INa was also observed with bepridil. The IC50 values of bepridil for depression of ICa and INa were 1.55 microM and 4.43 microM, respectively. 3. The muscarinic acetylcholine-receptor-operated potassium current (IK.ACh) was activated by the extracellular application of 1 microM carbachol in the GTP-loaded cells or by the intracellular loading of GTP gamma S, a nonhydrolysable GTP analogue. SD-3212 potently inhibited the carbachol- and GTP gamma S-induced IK.ACh and the IC50 values were 0.38 microM and 0.20 microM, respectively. These IC50 values were very close and about 10 times lower than those for inhibiting ICa and INa. Bepridil also suppressed the carbachol- and GTP gamma S-induced IK.ACh with the IC50 values of 0.69 microM and 0.84 microM, respectively. 4. In guinea-pig atrial cells stimulated at 0.2 Hz, carbachol at a concentration of 1 microM markedly shortened action potential duration. Both SD-3212 (0.1-1 microM) and bepridil (1-10 microM) reversed the action potential shortening in a concentration-dependent manner. The antagonizing effect of SD-3212 on the carbachol-induced action potential shortening was more potent than that of bepridil. 5. These results suggest that SD-3212 inhibits IK.ACh by depressing the function of the potassium channel itself and/or associated GTP-binding proteins. SD-3212 is a unique antiarrhythmic drug, which potently inhibits IK.Ach in addition to its class I and IV effects. SD-3212 and bepridil may be useful for the termination and prevention of vagally-induced atrial flutter and fibrillation.
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PMID:SD-3212, a new class I and IV antiarrhythmic drug: a potent inhibitor of the muscarinic acetylcholine-receptor-operated potassium current in guinea-pig atrial cells. 859 Oct

A retrospective review was done to determine the efficacy and hemodynamic effects of slow intravenous amiodarone administration on invasively monitored patients with acute onset of atrial fibrillation or atrial flutter and left ventricular ejection fractions < 15%. Eight patients met predefined inclusion criteria. All received 300 mg amiodarone intravenously over 1 hour. Seven reverted to sinus rhythm within 1 hour, with return of most hemodynamic variables to baseline. Before reversion, each patient experienced a beneficial slowing of heart rate (mean, 28%) resulting in significant improvement of stroke volume index (mean, 49%) and left ventricular stroke work index (mean, 61%). No patient had hemodynamic deterioration attributable to amiodarone infusion. Slow intravenous infusion of amiodarone appears to be an effective and hemodynamically well-tolerated therapy for atrial fibrillation and atrial flutter in critically ill patients with marked depression of left ventricular systolic function.
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PMID:Intravenous amiodarone for therapy of atrial fibrillation and flutter in critically ill patients with severely depressed left ventricular function. 870 76

Exhaustion occurs in most equestrian sports, but it is more frequent in events that require sustained endurance work such as endurance racing, three-day eventing, trial riding, and hunting. Exhaustion is also more likely when an unfit, unacclimatized, or unsound horse is exercised. Mechanisms that contribute to exhaustion include heat retention, fluid and electrolyte loss, acid-base imbalance, and intramuscular glycogen depletion. Clinical signs include elevated temperature, pulse, and respiratory rate; depression; anorexia; unwillingness to continue to exercise; dehydration; weakness; stiffness; hypovolemic shock; exertional myopathy; synchronous diaphragmatic flutter; atrial fibrillation; diarrhea; colic; and laminitis. Treatment includes stopping exercise; rapid cooling; rapid large volume intravenous or oral fluid administration; and nonsteroidal anti-inflammatory drug administration.
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PMID:The exhausted horse syndrome. 956 96

Electrocardiographic abnormalities had been reported, in patients with subarachnoid hemorrhage, with variable percentage from 2% to 91%, according to several studies. The most common changes are T wave inversion, ST segment elevation or depression, QT prolongation, U waves, atrial flutter and fibrillation, ventricular fibrillation, supraventricular tachycardia, premature atrial and ventricular contractions. These findings occur within the first forty-eight hours after the onset of the symptoms; they usually are benign and transient. In a small percentage of cases generally in severe ESA, the ECG changes are associated with ventricular asynergy, coronary vasospasm or subendocardic necrosis. The arrhythmias could be produced either by autonomic discharges to the heart, during increased sympathetic activity due to ESA, or by a damage of cerebral areas with arrhythmogenic capacity. The importance of ECG abnormalities towards mortality and morbidity in patients with ESA has not yet been cleared; however, a careful monitoring is recommended to prevent severe cardiac complications and to obtain an indirect, further evaluation of the neurologic pathology.
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PMID:[Subarachnoid hemorrhage and the heart]. 977 66

It's been said that major, landscape-changing events can sometimes stem from the humblest of origins: The gentle flutter of a butterfly's wings, the theory states, can begin a sequence of events that profoundly alters the weather pattern of an entire continent. In the world of science, this phenomenon is known as "chaos theory." But in the dynamic environment of the U.S. health care system--where the HMO philosophy has profoundly alter the way health care is delivered and financed--it has another name: Kaiser Permanente. From the humble yet revolutionary idea of a young surgeon caring for Depression-era workers in the Mojave Desert, to the current 6.7-million-member organization that has served as a model for plan administrators and policy makers across the country, Kaiser Permanente has originated, endured, and contributed more to the health care marketplace over the past 50 years than probably any other entity. Now, on Kaiser Permanente's golden anniversary, as the health plan reflects on its accomplishments and influence, it is plotting a course for quite challenging times ahead.
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PMID:Fifty years of caring. Kaiser Permanente turns 50 this year. 1016 80

Variable incidences of cardiac arrhythmias (based on isolated 12 lead ECG records) have been reported in patients of aluminium phosphide (ALP) poisoning. We did continuous holter and cardioscopic monitoring in ICU in 30 patients of acute ALP poisoning. Supraventricular and ventricular ectopics were recorded in each and every patient. Life threatening ventricular tachycardia was recorded in 40% cases and ventricular fibrillation in 23.3% cases. Supraventricular tachycardia and atrial flutter/fibrillation occurred in 46.7% and 20% patients, respectively. ST-T changes simulating myocardial ischaemia were also present in all patients (S-T depression in 90%, S-T elevation in 10%). One-third of the patients developed variable degrees of heart block, IV amiodarone/xylocard could revert dangerous ventricular arrhythmias to sinus rhythm in 4 cases. Toxic myocarditis produced by phosphine seems to be responsible for the development of these arrhythmias.
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PMID:Cardiac arrhythmias in aluminium phosphide poisoning studied by on continuous holter and cardioscopic monitoring. 1215 39

Fifty consecutive elderly (> 60 years) patients admitted to our department with congestive heart failure (CHF) entered a prospective database, to define their main clinical, instrumental and cognitive characteristics. In addition we evaluated the patterns of drug therapy in this aged population. Eighty percent of this sample had been previously hospitalized for CHF. Two or more associated diseases were present in 92%. Heart disease was ischemic or hypertensive in etiology in 80% of patients. Acute dyspnea was the most common presenting symptom. Atrial fibrillation or flutter were found in 38% of patients. Ultrasound evaluation evidenced left ventricular dysfunction of a systolic type in 49% and of a diastolic type in 28.6% of subjects. Diuretics and cardiac glycosides were the most widely administered drugs, followed by ACE-inhibitors, nitrates and dobutamine. Older ( >or= 75 years) patients were treated with more agents, with a trend to a lesser use of dobutamine. Moderate to severe mental deficit was present in 20.8% of our sample, while significant depression was more common (54.2%). The main implications of the clinical profile of the elderly patient hospitalized for CHF are discussed.
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PMID:Congestive heart failure in the elderly requiring hospital admission. 1537 42


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